title: [Cerebral amyloidosis].
abstract: Cerebral amyloidoses affects only the central nervous system, with rare exceptions. Most of them are related to A beta deposits. They usually occur in the absence of genetic defect in the precursor of A beta. The prevalence and density of A beta deposits increase during the aging process, and in Alzheimer's disease. This A beta amyloidosis has never been transmitted. In contrast, PrPres occurs as a sporadic or genetic event, and induces transmissible amyloidoses (Creutzfeldt-Jakob's disease and other disorders related to non conventional agents). PrPres may be the infectious agent itself (prion hypothesis). Other proteins are rarely responsible for cerebral amyloidoses. The fascinating hypothesis that a common mechanism would be acting in all cerebral amyloidoses has not yet been confirmed.
authors.affiliation: Laboratoire de neuropathologie, Raymond-Escourolle, Université Pierre et Marie Curie (Paris VI), INSERM U 360, Association Claude-Bernard, Paris.
authors.forename: Y
authors.initials: Y
authors.lastname: Grignon
authors.forename: M A
authors.initials: MA
authors.lastname: Colle
authors.forename: J J
authors.initials: JJ
authors.lastname: Hauw
mesh_terms: D017772:Amyloid Neuropathies / Q000139:chemically induced* / Q000175:diagnosis; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016657:Cerebral Amyloid Angiopathy / Q000175:diagnosis* / Q000378:metabolism; D006801:Humans; D011328:Prions / Q000009:adverse effects
chemical_list: D016229:Amyloid beta-Peptides; D011328:Prions
vernacular_title: Amylose cérébrale.